Summary
A variety of anesthetic techniques are used for facial plastic procedures. Laser treatment of facial lesions is a subset of these procedures that require unique considerations and planning. Procedural anesthesia and laser treatment may both be performed by the same practitioner; anesthesia of the region to be treated may be accomplished in a short period of time or can take an extended period of time requiring dedicated preprocedural preparation; procedures that require deep levels of sedation will require nursing staff and anesthesia personnel; and finally, there are numerous safety considerations unique to laser therapy that may dictate the type of anesthesia provided. Patient factors to consider include type and extent of lesions to be treated, overall health status of the patient, and prior experiences with laser treatment or other procedures requiring anesthesia. The type of anesthesia approaches needed can range from noninvasive methods using topical agents to invasive techniques that require infiltration of anesthesia with or without the addition of sedation (monitored anesthesia care [MAC]) to the use of general anesthesia in certain situations. 1 In this chapter, we discuss the commonly used anesthesia methods that are employed in treating laser resurfacing patients and review potential complications associated with these anesthetic techniques.
2 Anesthesia for Minimally Invasive Facial Aesthetic Surgery
2.1 The Office-Based Surgery Setting
The number and complexity of elective surgical procedures performed outside the hospital setting in the United States has expanded rapidly in the last 30 years. Part of the reason for this growth is the development of newer surgical and anesthesia techniques that allow more invasive and complex procedures to be performed safely in ambulatory surgery centers and in surgeons’ offices. 2 Following this trend, facial aesthetic surgery procedures are being routinely performed in the office-based settings. 3 In 2017, 17.5 million cosmetic procedures were performed in the United States. Out of these, 15.7 million or 70% were cosmetic minimally invasive procedures that were mostly done in the office. 4
Office-based surgery (OBS) and anesthesia offer many advantages to both patients and their healthcare providers. Procedures can be more conveniently and economically done in the office setting compared to the hospital. Patients get more personal attention and privacy, while surgeons enjoy more flexibility in scheduling and greater productivity. 5
For OBS facilities, regulations differ compared to hospital-based surgical facilities. Regulations vary from state to state and at the local government level. 5 The American College of Surgeons (ACS) issued guidelines listing ten core patient safety principles for OBS in a joint consensus statement with the American Medical Association (AMA) in 2003. 6 One principle requires that OBS facilities be accredited by one of a number of recognized regulatory organizations. The American Academy of Facial Plastic and Reconstructive Surgery, the American Society of Plastic Surgeons (ASPS), and the American Society of Aesthetic Plastic Surgery have mandated its members perform outpatient surgery only in accredited facilities for procedures needing intravenous and/or general anesthesia. Surgical cases that require local anesthesia and possibly some oral sedation are exempt. 7
2.2 Preprocedure Preparation
The ideal patient for a procedure performed in an office-based facility or ambulatory surgery center should have few or no comorbidities to avoid anesthesia complications. 8 The American Society of Anesthesiologists (ASA) Physical Status Classification status of I or II are associated with the lowest 30-day morbidity and mortality rates. 8 Patients with higher physical status ratings, associated with significant systemic disease, are considered poor candidates for deep sedation and general anesthesia and include patients with morbid obesity, obstructive sleep apnea, congestive heart failure, recent myocardial infarction (within the last 6 mo), severe chronic obstructive pulmonary disease, seizure disorder or stroke within the last 3 months. 8
Patients undergoing procedures involving the face may be more anxious and concerned than the general patient population. Discussions about pain management, expectations of pain levels, and patient’s prior experiences with procedural pain are increasingly appreciated as important to overall patient satisfaction. 9 Recent studies have shown communication about postoperative analgesia to be associated with decreased opioid consumption after procedures. 9 Patients who received preoperative education (including materials about pain control and opioids) were less likely to fill narcotic prescriptions, using non-narcotic analgesia more often than a comparison group receiving no preprocedure pain counseling. Pain scores of the counseled group were also lower postoperatively compared to the alternate group. 9
2.3 Local Anesthesia
Laser treatment of the skin of the face can be performed using local anesthesia with or without oral sedation that can be provided by the surgeon. 10 MAC with moderate-to-deep intravenous or general anesthesia administered by an anesthesiologist is employed for more extensive procedures. 11
Local anesthetics (LAs) are used to block transmission of nerve impulses, thereby reducing or eliminating sensation. 8 , 12 LAs may be applied topically, injected via subcutaneous tissue infiltration, injected to perform specific peripheral nerve blocks of the face, and used for tumescent anesthesia of the areas to be treated. 10 , 13 , 14 , 15
LAs are divided into esters and amides based on the chemical structure of the compounds. The majority of LAs in use are in the amide class (lidocaine, bupivacaine, ropivacaine, levobupivacaine, prilocaine) while cocaine and tetracaine are types of esters. 8 , 10 The metabolism of an LA differs between ester and amide classes. 10 , 12 , 13 The most commonly used LAs are lidocaine and bupivacaine (Table 2.1). Lidocaine has a duration of action of 2 to 3 hours compared to a longer duration of action of bupivacaine (3–8 h, prolonged duration with the addition of epinephrine). In the 1990s, two additional long-acting amides were introduced: levobupivicaine and ropivacaine which are the S-isomers of bupivacaine, a racemic mixture of S and R isomers. 12 These new agents—similar in potency, onset of action, and duration of effect to bupivacaine—have decreased central nervous system and cardiac toxicities. 16 The cardiac toxicity associated with bupivacaine plasma levels at toxic doses can be resistant to treatment with reported fatalities. 16
Esters are hydrolyzed by plasma cholinesterase while amides are metabolized by the cytochrome P450 system in the liver. 8 , 12 Any condition that reduces hepatic enzymatic function or hepatic blood flow can delay the metabolism and prolong the duration of action of amides. The dose of LA must be reduced in these patients. 8 , 12 LAs differ in their potency, onset and duration of action, and potential for toxicity. Several injectables are combined with epinephrine which increases the dose that can be safely given 10 (Table 2.1).
Anesthetic agent | Maximal dose (mg/kg) | Onset of action | Duration of action (h) |
Lidocaine 1% (10 mg/mL) | 5 | Rapid | 1.5–2 |
Lidocaine 1% + epinephrine | 7 | Rapid | 2–3 |
Bupivacaine .25% (2.5 mg/mL) | 2 | Slow | 3–6 |
Bupivacaine, 25% + epinephrine | 3 | Slow | 6–8 |
Bupivacaine .5% (5 mg/mL) | 2 | Slow | 3–6 |
Ropivacaine .5% (5 mg/mL) | 3 | Moderate | 3–8 |
Levobupivacaine .5% (5 mg/mL) | 3 | Moderate | 3–8 |
Source: Used with permission from Armstrong. 18 |
Allergic reactions to LAs are rare and many reactions described by patients as allergies most likely are idiosyncratic nonallergic reactions such as vasovagal and anxiety reactions. The reactions to additives such as epinephrine (flushing, palpitation) are often misconstrued or interpreted as allergies. 8 , 10 True allergies from LAs are from type I and IV hypersensitivity reactions. Anaphylaxis and immediate allergic reactions are examples of type I reactions, which typically begin within 1 hour after drug administration, but are very rare. Contact dermatitis and delayed-onset localized swelling are examples of type IV, delayed-type hypersensitivity reactions. Symptoms develop 1 to 3 days after drug administration and can be evaluated with patch testing. Allergic reactions to amide LAs are extremely rare, with the ester class of LAs most often the cause of allergies in patients. 8 , 12 One special circumstance can be encountered in patients who report allergies to sunscreen and other cosmetics. These products contain methylparaben—a preservative that is contained in some amide LAs and is metabolized to para-amino-benzoic acid (PABA). PABA can bind to tissue protein that is antigenic and can cause allergic dermatitis. PABA is also a metabolite of ester LAs. 8 , 12 Because of this common pathway, cases of cross-sensitization between ester and amide LAs have erroneously been reported. 8 , 12 , 13 If a patient is allergic to an ester-type LA, the patient should be given preservative-free amide. Proper screening with appropriate tests for ester or amide preservatives is important to clarify the basis for allergic reactions to LAs. 8 , 12 , 13
2.3.1 Topical Local Anesthesia
EMLA Cream
Eutectic mixture of local anesthetics (EMLA) is a topical anesthetic cream that contains a mixture of two amide LAs: 2.5% lidocaine and 2.5% prilocaine. 10 , 17 It is used to provide sensory anesthesia to intact normal skin. Its depth of penetration is 3 mm at its peak effect of 60 minutes and up to 5 mm after 1.5 to 2 hours. It is recommended that 2 g of EMLA cream be applied per 10 sq. cm of skin and covered with occlusive dressing for 60 minutes to attain adequate anesthesia for dermal procedures. 10
Known sensitivity to lidocaine, prilocaine, or other amide LAs and any predisposition to methemoglobinemia such as glucose-6-phosphate dehydrogenase deficiency are contraindications to the use of EMLA. 17 Most reactions associated with EMLA are mild, transient skin irritations. However, adverse reactions including methemoglobinemia can occur if EMLA is applied to large areas of skin for prolonged periods of time. 8 , 12
Liposomal Lidocaine
Liposomal lidocaine (LMX) is a topical cream preparation with a prolonged period of drug absorption and delay in its metabolism. LMX comes in two preparations: either 4% lidocaine (LMX 4) or 5% lidocaine (LMX 5). 1 The mechanism of action and effectiveness is similar to EMLA but it has a more rapid onset of analgesia than EMLA and its application does not require an occlusive dressing. Adequate anesthesia can be attained within 30 minutes after application. Contraindications for LMX include lidocaine hypersensitivity or allergy to any amide-type LA.
2.3.2 Subcutaneous or Tissue Infiltration
Lidocaine is the most commonly used anesthetic for local infiltration. It is usually given as a 1% solution (10 mg/mL). If large volumes are needed or a smaller dose is desired, the clinician may use a 0.5% solution. Large volume tissue infiltration should be executed in a way that does not distort tissue anatomy or obscure treatment landmarks. Needle gauge and injection technique are important factors in the pain associated with injections of local anesthesia. 10 Slow rates of injection decrease pain associated with infiltration. 10 , 11 Distraction techniques have been shown to decrease the anxiety and discomfort that patients experience during injection of local anesthesia. Tactile stimulation of the injection site by the injector or with a handheld vibratory device help distract the patient and decrease the stimulus perceived by the central nervous system. 8 Verbal distraction focusing and breathing techniques by the patients are other adjuncts that can be employed to deal with the anxiety of the injection. 10
Buffering of lidocaine with sodium bicarbonate decreases the pain of injection, and can shorten the time to anesthetic effect. 14 The basis for these effects is the increased pH of the solution from the addition of bicarbonate. 18 A ratio of 9 mL of lidocaine (with or without epinephrine) to 1 mL of 8.4% sodium bicarbonate is recommended. 10 , 18 , 19 A systematic review of randomized trials comparing levels of pain between patients receiving plain lidocaine and buffered lidocaine showed significantly decreased discomfort when bicarbonate was added to the LA. 18 Adding bicarbonate to bupivacaine may result in precipitation of the medications. 10 , 18 , 19
Local anesthetic systemic toxicity (LAST) stems from administration of large doses of LA. Increased plasma levels from local infiltration or inadvertent intravascular injection can result in adverse reactions. Initial signs of toxicity involve the central nervous system (CNS) including circumoral numbness, tinnitus, and agitation. Progession results in seizures and CNS depression with respiratory depression. 20 Cardiac toxicity initially manifests as tachycardia and hypertension, progressing to arrhythmias and cardiopulmonary collapse. 8 , 12 , 20 Treatment of systemic toxicity begins with support of the airway and blood pressure which may require the initiation of ACLS protocols. Benzodiazepines are a first-line therapy for seizures. 21 Cardiac arrhythmia secondary to local anesthesia toxicity, with bupivacaine toxicity being most refractory to treatment, can be treated with lipid rescue therapy. 12 , 20 Lipid emulsion therapy (administered intravenously) acts to bind and sequester plasma anesthetic. It should be administered at the first signs of LAST. 12 , 20